Asthma is characterized by airway inflammation, bronchial hyperresponsiveness and airflow obstruction. The development of symptoms in patients with asthma is initiated by exposure to a variety of airborne substances including aeroallergens. The inhalation of these allergens by asthmatic subjects initiates a series of complex, interactive immune events through activation of cell bound IgE, which serve to further existing airway inflammation, intensify underlying airway hyperresponsiveness and cause airflow obstruction. Although the immune events and processes associated with these reactions are largely localized to the airways themselves, a variety of other factors can contribute to the ongoing allergic response in either an enhancing or inhibitory manner. The regulation and modulation of these inflammatory actions is a key determinant to the eventual severity of asthma.